Anti-Aging Research, according to Tom Mahoney

Brian Manning Delaney bmdelaney at notarealaddr.ess
Mon Sep 28 16:28:25 EST 1998



This discussion of the merits of investigating the
mechanisms of CR vs. investigating telomeres is becoming
banal. It's degenerating into -- it perhaps was all along --
mere cheerleading.

To Tom Mahoney: Please try to be consistent in the yardstick
you choose to measure the success of an aging intervention.
In response to my post of Fri, 18 Sep 1998 21:18:29 GMT
["Subject: Re: Antiaging Research Priorities [was Re: Major
Criticisms of", Message-ID:
<3602CE24.D5124557 at notarealaddr.ess>], you wrote:

> The point I would
> make is that  all CR mice, of the same species,
> have the same life span.  This means that  CR
> has not altered the underlying genetic cause of
> aging.

By shifting the criteria of success to the alteration of the
_genetic_ cause of aging you're begging one of the very
questions that were on the table in this discussion.

And, by the way, you appear to have missed the point of the
hypothetical examples in my earlier posts, examples which
were designed to ferret out what you actually mean by
maximum life span. No matter, we now seem to have a working
definition -- "that achievable without researcher
intervention" -- which, while somewhat flawed, will be good
insofar as it's something we can all agree to stick to,
notwithstanding explicit qualifications of the definition.
(Tho' more on the definition in a moment.)


In a recent response to Tom Matthews, you wrote, once again
arguing that CR experiments haven't increased maximum life
span:

> Organisms in the  wild do experience food
> shortages and the closer these shortages are to
> the CR diet the longer these organisms will
> live by adopting the responses demonstrated in
> the CR research. 

If you want to argue that percentage gains in maximum life
span reported in CR studies are slightly too high, you'll
get no heated argument from me. Maybe instead of 50%, we
should call them 40% or even 35%. As you point out to Tom
Matthews (deleted), the control conditions are artificial
too. (The standard response to you would be: most mice in
the wild don't have _nearly_ so well as overfed lab rats.
But that would miss your point, I agree.)

To say, however, as you have been doing, that CR doesn't
increase the maximum life span of rodents AT ALL is without
warrant.

I explained why I think this is the case before, by claiming
that CR almost certainly does not occur in the wild for more
than very brief periods (food restriction occurs for more
than brief periods). You responded (message
<6tuq9o$lhf$1 at birch.prod.itd.earthlink.net>):

> As to the mice, while I agree that is the most
> likely scenario but we are  looking for the
> extraordinary mouse that lived the longest who
> probably came  pretty close to mimicking CR as
> used in the Labs. to determine maximum life  span.

I never responded to this, since it was clear by your
failure to respond to my hypothetical examples that your
mind wasn't in a position to be changed on this score.

I'm going to try again, briefly.

Let's consider the definition of maximum life span given
above. You're using this definition in a very strange way.
You don't even see the need to find the longest lived
natural animal on which your definition of maximum life span
is based. You're simply ASSUMING that this "extraordinary
mouse" is out there, or was out there, or could be out
there.

Thus, your definition of maximum life span seems to be: "the
life span achievable without researcher intervention in any
extraordinary circumstances we can imagine possibly existing
in nature, even if we haven't actually encountered such
circumstances."

This seems a rather forced definition.

Let me return to one of my earlier hypothetical examples:

BMD> Take another example. Say we had evolved a
BMD> mechanism whereby eating a certain substance
BMD> found in a now rare plant turns on telomerase in
BMD> enough cells, in the right way, to slow aging.
BMD> No one has been known to eat the substnce
BMD> because our dietary habits over the last few
BMD> centuries have precluded its consumption. But
BMD> suddenly we discover it, and people start taking
BMD> it and living to be 140 years old. Since this
BMD> ability to age slowly under the conditions of
BMD> the presence of this substance is an
BMD> evolutionary adaptive response, would you say
BMD> people living to 140 by means of this substance
BMD> aren't extending their life span?

You responded by saying I had "changed the premise" by
stipulating that humans would live to over ~120, and that
therefore such a substance WAS increasing maximum life span.

Then you changed your mind, and came to agree with the
definition of maximum life span we've been working with: the
"non-intervened" life span. So then, with the discovery of
this substance, we wouldn't be altering the maximum life
span of humans, you would argue, because researchers
wouldn't be needed to produce the change (since the
substance is natural, and naturally availalbe).

Do you really think that makes sense?

What about if the substance turned on telomerase -- again,
by means of a genetic potential already existing which
permitted such a turning-on via the substance -- in a way
that enabled us to live to 200? Not increasing maximum life
span here, either? That would be an odd claim, odd in its
lack of general utility. A cynic would of course say, "Yes,
but the goal for Tom isn't _general_ utility, but rather
utility in specifically this: raising funds for Tom Mahony's
anti-aging venture." Let us then prove the cynics wrong!

Your recent response to Tom Matthews, quoted above, suggests
to me that you, at bottom, don't fully agree with the
"non-intervened" definition of maximum life span. It's not a
perfect definition, to be sure. But perhaps you should
pause, and work through just what it is you take a
reasonable definition of maximum life span to be. We should
all do that. It's obviously a very complicated issue.

<>

One last thing:

Please don't say things that are false, or very misleading,
when you almost certainly know better, like this:

> The beneficial effects of CR, including the
> suppression of mitotic  activities, is related
> to a decrease in body temperature in both mice
> and  Rhesus monkeys.

There was ONE study, not yet repeated, that showed that some
of the beneficial effects of CR are abolished when ambient
temperature is raised, in RODENTS. We have NOTHING to
support the idea that this would happen with monkeys on CR.
The finding that monkeys' body temperature is lowered on CR
does not bear in any empirical way on this. We would need to
change the ambient temperature and see what happens. This
hasn't been done.

Best,
Brian.
--
Brian Manning Delaney
My email address is here:
http://xyz.uchicago.edu/users/bmdelane/email4.htm
[Wrists: "Leave unambiguous typos."]
Note: All statements in this article are in jest; they
are not statements of fact.
"Mein Genie ist in meinen Nuestern." -Nietzsche.
** Please do not CC your Usenet articles to me. I'll find
them.




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